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Biomedical subjects

T Zhang

Publications and source records attributed to T Zhang.

At least 325 records · Page 18Linked to original sources
PubMed1996

[Cluster epithelial cells in nasal secretions of allergic rhinitis and its relation to eosinophils].

The cytology of nasal secretions in 20 patients with allergic rhinitis and 15 patients with chronic maxillary sinusitis was investigated with transmission electron microscope to study the ultrastructure of the cluster epithelial cells in nasal secretions of allergic rhinitis. The results showed that the cluster epithelial cells were predominant cellular element in allergic nasal secretions. The number of cluster cells correlated positively with the number of eosinophils and the levels of eosinophilic cationic protein. It is suggested that the exfoliation of cluster nasal epithelial cellular elements may be caused by eosinophic cationic protein with resultant hyperreactivity of nasal mucosa.

Adolescent↗
PubMed1995

Downregulation of prohormone convertase-1 by a phorbol ester.

Acute TPA treatment (1h, 100nM) of a human pancreatic carcinoid cell line (BON) depletes cell contents of chromogranin A (CGA) and pancreastatin (PST), a peptide derived posttranslationally from CGA. Despite removal of TPA, BON cells continue to release CGA in an unregulated fashion whereas PST secretion is reduced substantially. TPA treatment also reduced prohormone convertase-1 (PC-1) protein and increased PC-1 mRNA levels. Together, these findings indicate that the TPA-induced switch from a regulated to unregulated pattern of CGA secretion is accompanied by a decrease in the processing of CGA to PST and a decrease in the active form of a processing enzyme potentially involved in processing CGA to a smaller peptide, PST.

Aspartic Acid Endopeptidases↗
PubMed1995

Comparison of inactivation and conformational changes of aminoacylase during guanidinium chloride denaturation.

The inactivation and unfolding of aminoacylase (EC 3.5.1.14) during denaturation by different concentrations of guanidinium chloride (GuHCl) have been compared. A marked decrease in enzyme activity is already evident at low GuHCl concentrations before significant unfolding of the enzyme molecule, as monitored by fluorescence, ultraviolet difference absorption and CD measurement. The kinetic theory of the substrate reaction during irreversible inhibition of enzyme activity previously described by Tsou has been applied to a study on the kinetics of the course of inactivation of aminoacylase during denaturation by GuHCl. The inactivation rate constants of free enzyme and substrate-enzyme complex were determined by Tsou's method. The inactivation reaction kinetics were found to be a monophasic first-order reaction. The kinetics of the unfolding were a bisphasic process consisting of two first-order reactions. At lower GuHCl concentration (< 1.0 M), the enzyme activity was stripped at a high rate whereas its conformation was only slightly affected. At 1.0 M GuHCl, the inactivation rate of the enzyme was much faster than the unfolding rate. At higher GuHCl concentrations (> 1.0 M), the inactivation rate was too fast to be measured by conventional dynamic methods, whereas the unfolding remained as a bisphasic process with the fast reaction accruing very fast and the slow reaction occurring at a measurable rate. The results suggest that active sites of aminoacylase containing Zn2+ ions are situated in a limited region of the enzyme molecule that is more fragile to denaturants than the protein as a whole.

Amidohydrolases↗
PubMed1995

The size of the anterior spinal artery in relation to the arteria medullaris magna anterior in humans.

We studied the anterior spinal artery (ASA) in 25 cadaveric human spinal cords to determine the cross-sectional area of the ASA cephalad and caudal to the entry of the arteria medullaris magna anterior (AMMA). Spinal cords were removed en bloc and latex was injected into the AMMA. The preparations were then fixed in formalin, embedded in paraffin, sectioned, mounted, and stained with hematoxylin and eosin. The diameter and cross-sectional area of the ASA 1 cm above and 1 cm below the entry of the AMMA were measured. The mean radius of the ASA above the entry of AMMA was 0.14 +/- 0.03 mm compared to 0.28 +/- 0.05 mm below the entry of the AMMA (P < 0.001). According to Poiseuille's equation, the resistance to blood flow in the ASA cephalad to the AMMA would be 14.8 times greater than the resistance to blood flow caudal to the AMMA. This resistance could affect the distribution of blood flow in the distal spinal cord whenever flow in the AMMA or distal ASA is altered.

Adult↗
PubMed1995

Modeling substrate binding in Thermus thermophilus isopropylmalate dehydrogenase.

The Thermus thermophilus 3-isopropylmalate dehydrogenase (IPMDH) and Escherichia coli isocitrate dehydrogenase (ICDH) are two functionally and evolutionarily related enzymes with distinct substrate specificities. To understand the determinants of substrate specificities of the two proteins, the substrate and coenzyme in IPMDH were docked into their respective binding sites based on the published structure for apo IPMDH and its sequence and structural homology to ICDH. This modeling study suggests that (1) the substrate and coenzyme (NAD) binding modes of IPMDH are significantly different from those of ICDH, (2) the interactions between the substrates and coenzymes help explain the differences in substrate specificities of IPMDH and ICDH, and (3) binding of the substrate and coenzyme should induce a conformational change in the structure of IPMDH.

3-Isopropylmalate Dehydrogenase↗
PubMed1995

Increased locus coeruleus glutamate levels are associated with naloxone-precipitated withdrawal from butorphanol in the rat.

Extracellular fluid levels of glutamate were measured in the locus coeruleus during butorphanol (a mixed agonist at mu-, delta-, and kappa-opioid receptors) withdrawal by using microdialysis in conscious butorphanol-dependent Sprague-Dawley rats. Guide cannulae were implanted chronically and rats were given intracerebroventricular (i.c.v.) infusions of butorphanol (26 nmol/1 microliter/hr) or saline (1 microliter/hr) for 3 days. Microdialysis probes (2 mm tip) were inserted into the locus coeruleus 24 hr before precipitation of withdrawal by i.c.v. injection of naloxone (48 nmol/5 microliters). A separate series of rats was rendered dependent by peripheral injection of butorphanol (20 mg/kg, s.c., b.i.d.) for 5 days and naloxone (5 mg/kg, i.p.) was given to precipitate withdrawal. Single injections of butorphanol (26 nmol/5 microliters, i.c.v.) had no effect on the extracellular fluid levels of glutamate, compared to rats injected with vehicle. Behavioral evidence of withdrawal was detected following naloxone challenge in butorphanol-dependent rats (both i.c.v. and s.c. models), but not in non-dependent, vehicle-treated rats. Significant increases (P < 0.05) in levels of glutamate were noted after naloxone-precipitated withdrawal only in the butorphanol group. The glutamate levels in the locus coeruleus increased from 8.37 +/- 2.01 before, to 21.93 +/- 4.58 microM in the first 15 min sample following i.c.v. injections of 48 nmol/5 microliters naloxone and from 10.84 +/- 1.74 before, to 26.01 +/- 6.19 microM in the 15-30 min sample following i.p. injections of 5 mg/kg naloxone in the butorphanol-dependent rats, respectively. These results provide direct evidence to support the role of excitatory amino acids within the locus coeruleus in butorphanol withdrawal.

Animals↗
PubMed1995

Inactivation and unfolding of aminoacylase during denaturation in sodium dodecyl sulfate solutions.

During denaturation by sodium dodecyl sulfate (SDS), aminoacylase shows a rapid decrease in activity with increasing concentration of the detergent to reach complete inactivation at 1.0 mM SDS. The denatured minus native-enzyme difference spectrum showed two negative peaks at 287 and 295 nm. With the increase of concentration of SDS, both negative peaks increased in magnitude to reach maximal values at 5.0 mM SDS. The fluorescence emission intensity of the enzyme decreased, whereas there was no red shift of emission maximum in SDS solutions of increasing concentration. In the SDS concentration regions employed in the present study, no marked changes of secondary structure of the enzyme have been observed by following the changes in far-ultraviolet CD spectra. The inactivation of this enzyme has been followed and compared with the unfolding observed during denaturation in SDS solutions. A marked inactivation is already evident at low SDS concentration before significant conformational changes can be detected by ultraviolet absorbance and fluorescence changes. The inactivation rate constants of free enzyme and substrate-enzyme complex were determined by the kinetics method of the substrate reaction in the presence of inactivator previously described by Tsou [Tsou (1988), Adv. Enzymol. Related Areas Mol. Biol. 61, 381-436]. It was found that substrate protects against inactivation and at the same SDS concentrations, the inactivation rate of the free enzyme is much higher than the unfolding rate. The above results show that the active sites of metal enzyme containing Zn2+ are also situated in a limited and flexible region of the enzyme molecule that is more fragile to denaturants than the protein as a whole.

Amidohydrolases↗
PubMed1995

Plasma levels of beta-endorphin, leucine enkephalin and arginine vasopressin in patients with essential hypertension and the effects of clonidine.

In order to investigate the changes of endogenous opiate systems in hypertension and their possible role in the pathogenesis in hypertension, we measured plasma concentrations of beta-endorphin, leucine-enkephalin, neurotension, arginine vasopressin, plasma renin activity and angiotensin II by radioimmunoassay in 60 normal persons and 120 patients with essential hypertension. The results showed that the patient group had lower levels of beta-endorphin and leucine enkephalin (P < 0.001), higher levels of arginine vasopressin, plasma renin activity and angiotensin II (P < 0.01, P < 0.05 and P < 0.05, respectively), and normal level of neurotensin, as compared with those in normal group. Plasma levels of leucine-enkephalin was correlated negatively to the mean artery pressure (r = -0.196, P < 0.05). Plasma level of arginine vasopressin was correlated to the duration of the hypertension (r = 0.216, P < 0.05). After 150 min and 14 days of treatment with clonidine, plasma levels of beta-endorphin, leucine-enkephalin increased significantly (< 0.01) and correlated negatively with the decrease of the mean artery pressure (r = -0.340 and r = -0.436 at 150 min, r = -0.369 and r = -0.441 on the 14th day, respectively, P < 0.01). Plasma renin activity and angiotensin II decreased significantly (P < 0.05 and P < 0.01). Arginine vasopressin and neurotensin did not change significantly. After intravenous administration of opiate antagonist-naloxone, the blood pressure and heart rate increased significantly (P < 0.01). The results suggested that the changes of endogenous opioids may be involved in the pathogenesis of hypertension and in the antihypertensive action of clonidine.

Angiotensin II↗
PubMed1995

Immunogenicity of the recombinant serine rich Entamoeba histolytica protein (SREHP) amebiasis vaccine in the African green monkey.

We report the first study in non-human primates of the safety and immunogenicity of a recombinant vaccine designed to prevent amebic liver abscess. In a pilot study, a recombinant vaccine containing the serine rich Entamoeba histolytica protein (SREHP) attached to a maltose binding protein (SREHP/MBP), which has been shown to be effective in preventing amebic liver abscess in rodent models of infection, was used to immunize two African Green Monkeys. Vaccination with SREHP/MBP resulted in no systemic side-effects. The monkeys receiving the SREHP/MBP protein developed antibodies that recognized the recombinant SREHP/MBP molecule, the native SREHP protein, and the surface of amebic trophozoites. Antiserum from SREHP/MBP-vaccinated monkeys could block the adhesion of E. histolytica trophozoites to mammalian cells, a feature that may correlate with vaccine efficacy. Attempts to produce amebic liver abscess in naive African Green Monkeys by direct hepatic inoculation with virulent E. histolytica trophozoites was not successful, suggesting this species is probably not suitable for vaccine efficacy studies.

Animals↗
PubMed1995

RT/PCR detection of SIL-TAL-1 fusion mRNA in Chinese T-cell acute lymphoblastic leukemia (T-ALL).

The TAL-1 gene is located on chromosome 1p32. In about 20% of T-cell acute lymphoblastic leukemias (T-ALL), this gene is disrupted in its 5' portion by a site-specific 100-kg deletion and is fused with the 5' part of the SIL gene, to form SIL-TAL-1 chimeric gene. In this study, we established a "nested" retrotranscriptase/polymerase chain reaction (RT/PCR) technique which allows detection of the SIL-TAL-1 transcriptional expression. A chimeric mRNA was observed in four of 17 T-ALL cases and has been shown to result from the fusion between the exon 1 of SIL and exon 3 of TAL. A sensitivity test showed that this RT/PCR procedure could detect one leukemic cell among 10(6) normal cells. A positive RT/PCR result was obtained in two cases during clinical remission, suggesting the presence of minimal residual disease (MRD). One patient developed clinical relapse 3 months after PCR positivity. Moreover, analysis of the Tald rearrangement by DNA-based PCR in four patients with SIL-TAL-1 fusion revealed the type A (Tald1) rearrangement in all cases. Sequence analysis demonstrated the presence of N region and non-random "P" nucleotide, as well as base deletions at the genomic SIL-TAL-1 joining site. These data indicate that detection of TAL-1 gene abnormality is important for diagnosis and monitoring of MRD in a subset of T-ALL.

Adolescent↗
PubMed1995

Phenotypic and molecular analysis of a transgenic insertional allele of the mouse Fused locus.

Spontaneous mutations at the mouse Fused (Fu) locus cause dominant skeletal and neurological defects and recessive lethal embryonic defects including neuroectodermal abnormalities and axial duplications. Here, we describe a new allele at the Fu locus caused by a transgenic insertional mutation, H epsilon 46. Embryos homozygous for the H epsilon 46 insertion die at day 9-10 post coitum and display phenotypic defects similar to those associated with Fu alleles. The H epsilon 46 locus was cloned and shown to contain a 20-kb deletion at the site of transgene insertion with no other detectable rearrangements. Genomic probes from the H epsilon 46 locus were mapped to a genetic locus closely linked to Fu on chromosome 17 and were hybridized to a YAC contig covering the FuKi critical region. Compound heterozygotes between H epsilon 46 and FuKi were inviable and displayed abnormalities at the same stage of embryogenesis as do homozygotes for either of the two mutations, demonstrating that these two recessive lethal mutations belong to the same complementation group. A genomic probe from the wild-type H epsilon 46 locus detected a transcript that is disrupted by the transgenic insertion, representing a candidate for the wild-type allele of Fused.

Alleles↗
PubMed1995

Interaction of laminin with Entamoeba histolytica cysteine proteinases and its effect on amebic pathogenesis.

The Entamoeba histolytica 27-kDa cysteine proteinases exhibit striking binding specificities for immobilized laminin over other components of the extracellular matrix, such as collagen and fibronectin. Inactivation of the proteinase with the active-site inhibitor L-trans-epoxysuccinyl-leucylamido(4-guanidino)butane abolishes laminin binding by the enzyme, and conversely, laminin inhibits cleavage of a fluorogenic dipeptide substrate of the amebic cysteine proteinase, suggesting that the substrate binding pocket of the enzyme is involved in the binding of laminin. The addition of laminin but not fibronectin or collagen to E. histolytica trophozoites significantly reduces amebic liver abscess formation in severe combined immunodeficient mice, further supporting the hypothesis that E. histolytica cysteine proteinases play an important role in amebic pathogenesis. The specific interaction of amebic proteinases with laminin may be exploited in designing new inhibitors of these enzymes.

Amino Acid Sequence↗
PubMed1995

Oral immunization with the dodecapeptide repeat of the serine-rich Entamoeba histolytica protein (SREHP) fused to the cholera toxin B subunit induces a mucosal and systemic anti-SREHP antibody response.

The intestinal protozoan parasite Entamoeba histolytica causes amebic dysentery, a major cause of morbidity worldwide. The induction of a mucosal antibody response capable of blocking amebic adhesion to intestinal cells could represent an approach to preventing E. histolytica infection and disease. Here we describe the expression of a chimeric protein containing an immunogenic dodecapeptide derived from the serine-rich E. histolytica protein (SREHP), fused to the cholera toxin B subunit (CtxB). The CtxB-SREHP-12 chimeric protein was purified from Escherichia coli lysates and retained the critical GM1 ganglioside-binding activity of the CtxB moiety. Mice fed the CtxB-SREHP-12 fusion protein along with a subclinical dose of cholera toxin developed mucosal immunoglobulin A and immunoglobulin G and systemic antibody responses that recognized recombinant and native SREHP. Our study confirms the feasibility of inducing mucosal immune responses to immunogenic peptides by their genetic fusion to the CtxB subunit and identifies the CtxB-SREHP-12 chimeric protein as a candidate oral vaccine to prevent E. histolytica infection.

Administration, Oral↗